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INTERNATIONAL CONGRESS OF

CancerGenetics

• TLR3 Genetic Variation in Virus-Related Hepatocellular Carcinoma

• Parisa Gozali,¹ Abolfazl Barzegari,² Maryam Anari,³ Mohammad Reza Sadeghi,^4,*
  1. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
  2. Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
  3. Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
  4. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
  
  
  
• Introduction: Hepatocellular carcinoma (HCC) is an extremely aggressive cancer with few available treatment approaches (Li & Zheng, 2013). Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are the major causes of hepatocellular carcinoma (HCC), comprising most cases worldwide (Fung et al., 2009). Toll-like receptors (TLRs) are part of a powerful system for identifying and eliminating pathogen-associated molecular patterns (PAMPs) from bacteria and viruses (Kircheis & Planz, 2023). TLR3 binds viral double-stranded RNAs (dsRNAs) as pathogenic non-self and responds through upregulating its expression, enhancing IFN-β responses and inducing the release of inflammatory cytokines (Sartorius et al., 2021). Multiple studies have identified TLR3 expression in diverse malignancies, such as breast, prostate and lung cancer (Muresan et al., 2020). Genetic polymorphisms in TLR3 have been suggested as potential factors influencing susceptibility to viral infection and cancer development. Therefore, we summarize the evidence regarding the role of TLR3 +1234C/T polymorphism as a common host genetic signature across distinct viral etiologies of hepatocellular carcinoma.
• Methods: We searched the PubMed and Google Scholar databases using relevant keywords, including hepatocellular carcinoma, polymorphism and TLR3, to identify the original articles that involved TLR3 polymorphism and hepatocellular carcinoma.
• Results: Several studies have investigated the association between TLR3 +1234C/T polymorphism and susceptibility to virus-related HCC. In HBV-associated HCC, a study including 466 HCC patients and 482 healthy controls evaluated two TLR3 polymorphisms, -976T/A and +1234C/T. The results showed that the prevalence of the +1234CT genotype and +1234TT genotype was significantly increased in HCC cases compared with controls. Furthermore, HBV carriers with HCC showed a higher frequency of the +1234CT genotype and +1234T allele compared with individuals without HBV infection. These findings indicate that the TLR3 +1234C/T polymorphism could be a novel risk factor for HCC, especially HBV-related HCC (Li & Zheng, 2013). Similarly, the role of TLR3 +1234C/T polymorphism was investigated in HCV-related HCC among Egyptian patients. In this study, 50 HCV cirrhotic patients were divided into groups with HCC and without HCC and compared with healthy controls. The prevalence of the TLR3 +1234TT genotype was significantly increased in cirrhotic patients with HCC compared with those without HCC, while it was not detected among controls. In addition, the +1234TT genotype was significantly associated with the number of hepatic focal lesions, size and higher Okuda and BCLC stages in HCC patients (El-Sharawy et al., 2020).
• Conclusion: These findings suggest that the TLR3 +1234C/T polymorphism may represent a shared host genetic factor associated with hepatocellular carcinoma development across different viral etiologies. The presence of this genetic variant in both HBV-related and HCV-related HCC supports its potential role as a common susceptibility marker for virus-associated hepatocarcinogenesis.
• Keywords: Hepatocellular carcinoma, polymorphism, TLR3.